What's in Your Drink? Poster Educates Families About Sugar Content and Fatty Liver Disease.

OBJECTIVE: Drinking sugar-sweetened beverages is a risk factor for developing childhood obesity and nonalcoholic fatty liver disease (NAFLD). This study investigated the impact of an educational poster in pediatric offices on family's knowledge of sugar content in beverages and assessed awareness of NAFLD. DESIGN: Preclinic visit surveys asked patients' caregivers about the sugar content in beverages and awareness of NAFLD. Postclinic visit surveys assessed improvement in knowledge of sugar content and willingness to change dietary habits. SETTING: Outpatient visits in a single center in Houston between September and November 2019. PARTICIPANTS: One hundred and forty-nine caregivers were surveyed, and patients' median age was 5.5 years (range, 0-18 years) with 57% males. INTERVENTION: Educational posters displayed the sugar content of common beverages in each clinic room. MAIN OUTCOME MEASURES: Outcomes measured included pre-post clinic visit change and predictors of change in (1) knowledge of sugar content in beverages and (2) intent to change beverage consumption. Baseline awareness of NAFLD and associated predictors were also assessed. ANALYSIS: Logistic regression identified factors associated with an intended change in beverage consumption, change in survey score, and NAFLD awareness. RESULTS: Increased knowledge of sugar content with median scores of 25% preclinic to 50% postclinic (P < 0.001). Eighty-eight percent of caregivers were very/moderately likely to provide their children fewer sugar-sweetened beverages. Sixty percent of caregivers were aware of NAFLD, but only 32.8% were concerned. CONCLUSIONS AND IMPLICATIONS: Posters in clinics increased awareness of the sugar content in beverages, and most caregivers reported intent to decrease children's sugary beverage consumption.

Molecular mechanisms of functional natural killer deficiency in patients with partial DiGeorge syndrome.

BACKGROUND: DiGeorge syndrome affects more than 3.5 million persons worldwide. Partial DiGeorge syndrome (pDGS), which is characterized by a number of gene deletions in chromosome 22, including the chicken tumor virus number 10 regulator of kinase (Crk)-like (CrkL) gene, is one of the most common genetic disorders in human subjects. To date, the role of natural killer (NK) cells in patients with pDGS remains unclear. OBJECTIVE: We sought to define the effect of pDGS-related Crk haploinsufficiency on NK cell activation and cytotoxic immunological synapse (IS) structure and function. METHODS: Inducible CrkL-silenced NK cells were used to recapitulate the pDGS, CrkL-haploinsufficient phenotype. Findings were validated by using NK cells from patients with actual pDGS. Ultimately, deficits in the function of NK cells from patients with pDGS were restored by lentiviral transduction of CrkL. RESULTS: Silencing of CrkL expression inhibits NK cell function. Specifically, pDGS haploinsufficiency of CrkL inhibits accumulation of activating receptors, polarization of cytolytic machinery and key signaling molecules, and activation of ß2-integrin at the IS. Reintroduction of CrkL protein restores NK cell cytotoxicity. CONCLUSION: CrkL haploinsufficiency causes functional NK deficits in patients with pDGS by disrupting both ß2-integrin activation and activating receptor accumulation at the IS. Our results suggest that NK cell IS quality can directly affect immune status, providing a potential target for diagnosis and therapeutic manipulation in patients with pDGS and in other patients with functional NK cell deficiencies.